Tissue samples were obtained by performing liver biopsies on 30 participants with chronic HBV infection and 42 control patients.

Although activation of toll-like receptor 3 (TLR3) binding and Sendai virus infection in the liver induces an innate immune response among those infected with hepatitis B virus (HBV), liver tissues of patients infected with HBV generally do not exhibit an active innate immune response, according to study findings published in Gastroenterology.

Investigators obtained liver biopsies from patients with chronic HBV infection (hepatitis B e antigen-positive or hepatitis B e antigen-negative, with or without hepatitis, n=30) and control patients (n=42), the majority of whom had fatty liver disease. The investigators used histology, immunohistochemistry, quantitative reverse-transcription polymerase chain reaction, in situ hybridization, HBV RNA quantification, and HBV genotyping for evaluating the liver tissues. In addition, the researchers also infected some of the specimens with Sendai virus or incubated with TLR ligands before assessment.

The liver samples from HBV-infected patients did not express greater interferon (IFN) or IFN-stimulated genes compared with specimens from the control group, suggesting HBV infection itself was not associated with an activation of an innate immune response. After activation of TLR3 with poly(I:C) or Sendai virus infections, liver specimens of HBV-infected patients produced IFN and expressed IFN-stimulated genes, indicating that the innate immune response is not suppressed in liver tissue.

Because the investigators were unable to collect liver specimens from patients with acute HBV infection, the study was unable to determine whether active suppression of IFN-inducing sensory pathways or IFN signaling occurs in the early phases of HBV.

Findings from this study "support the hypothesis that HBV behaves like a stealth virus by staying under the radar of the pathogen detection system."